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Abstract
Müller radial glia accumulate glial fibrillary acid protein (GFAP) in response to retinal injuries. We have studied the changes in cellular localization of GFAP in genetically caused retinal dystrophy in strains of cat and mouse: Abyssinian cats with progressive retinal dystrophy, and mice homo- and heterozygous for the retinal degeneration (rd) and retinal degeneration slow (rds) genes. The following observations were made: (1) Glial fibrillary acid protein-immunoreactive (GFAP-IR) radial Müller glia are present in normal cat and mouse retinae. (2) There is a general increase with age in numbers of GFAP-IR radial Müller glia, and other GFAP-IR elements in the retina of cat and mice with hereditary retinal dystrophy. (3) The increase in GFAP-accumulating Müller cells seems to proceed from peripheral to central retina in both cats and mice. This might reflect the direction of photoreceptor degeneration, which proceeds in the same direction in the retinal dystrophic cat and in mice bearing the rds gene. However, in the rd mouse photoreceptor degeneration proceeds from central to peripheral retina, indicating that GFAP accumulation is not a local direct effect of photoreceptor damage. (4) Comparing the different mutant mouse strains, there seem to be qualitative differences in the distribution of GFAP-IR elements. The numbers of tangential elements and fibrillary tangles in the inner plexiform and nuclear layers are highest in the +/+ rds/rds retina, followed by the +/+ rds/+, whereas such elements appear to be more scarce in rd/rd rds/rds, followed by the rd/rd +/+ and +/+ +/+ retinae.(ABSTRACT TRUNCATED AT 250 WORDS)